Cell death is crucial for normal development, homeostasis, and the prevention of hyperproliferative diseases such as cancer. It was once thought that almost all regulated cell death in mammalian cells resulted from the activation of caspase-dependent apoptosis. Very recently this view has been challenged by the discovery of several regulated non-apoptotic cell death pathways activated in specific disease states. Regulated necrosis is defined as a genetically controlled cell death process that eventually results in cellular leakage, and is morphologically characterized by cytoplasmic granulation, as well as organelle and/or cellular swelling. An overview of these different regulated necrosis pathways is presented in T. Vanden Berghe et al. (2014) Nat. Rev. Mol. Cell. Biol. 15:135-147. Ferroptosis is one recognized form of regulated necrosis and its hallmark is the production of iron-dependent reactive oxygen species (ROS). Ferroptosis is partly mediated through inhibiting the system Xc− Cys/Glu antiporter, which allows the exchange of extracellular L-Cys and intracellular L-Glu across the plasma membrane. Ferroptosis involves metabolic dysfunction that results in the production of both cytosolic and lipid ROS, independent of mitochondria but dependent on NADPH oxidases. It is believed that ROS generated by Fenton-type reactions (dependent on the availability of catalytic ferrous iron), rather than the mitochondrial electron transport chain are the main drivers of ferroptosis. Glutathione (GSH) peroxidase 4 (GPX4) is a crucial inhibitor of ferroptosis, and its activity relies on GSH levels. Therefore, GSH depletion typically leads to loss-of-function of GPX4, resulting in ROS-mediated lipid peroxidation. In addition to ferroptosis, glutamine- and oxidative stress-induced cell death are inhibited by iron chelation. In line with this, iron-dependent neuronal cell death is blocked by metal protein-attenuating compounds (e.g., clioquinol) and iron chelators (e.g., desferroxamine), which are being explored for the treatment of neurodegenerative diseases. Another type of regulated necrosis is oxytosis which is also induced when the Xc− Cys/Glu antiporter is inhibited through an excess of the neurotransmitter glutamine, the latter process is often designated as excitotoxicity in neuronal cells. Because of the clear mechanistic overlaps between oxytosis and ferroptosis it is not excluded that the use of modulators of ferroptosis in disease will also target the same disease processes which are associated with oxytosis. Disease processes where undesired ferroptosis and/or oxytosis occur are typically disorders where an oxidative stress factor is involved such as, for example, in several neurodegenerative diseases, liver-, cardiac- and kidney-ischemia—reperfusion injury, stroke, sepsis, diabetes and epilepsy. Oxidative stress due to iron overload is, for example, highly relevant in organs accumulating iron such as the brain, kidney and liver. Several compounds have been described in the art which are able to inhibit ferroptosis such as, for example, WO2013/152039, R. Skouta et al. (2014) J. Am. Chem. Soc. 136:4551-4556, and A. Linkermann et al. (2014) www.pnas.org/cgi/doi/10.1073/pnas.1415518111). The prior art highlights the importance of the ethyl-ester in the maintenance of the potency of the first-in-class compound ferroptosis inhibitor molecule (designated as Ferrostatin-1) and suggests chain modifications of the ester, see Skouta et al. (2014), for generating improved molecules. Indeed, the latter reference also teaches that esters modified to amides at the same position have a lower EC50. In addition, Linkerman et al. (2014) also disclose that improved pharmacokinetic variants of Ferrostatin-1 should be ester analogs.